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Biomedicines
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Advances in Heart–Brain Axis
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Advances in Heart–Brain Axis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 19 February 2027 | Viewed by 8890

Editor

Dr. Teresa Soda

E-Mail Website
Guest Editor
Department of Health Science, Laboratory of Physiology and Neuropharmacology, University Magna Græcia of Catanzaro, 88100 Catanzaro, Italy
Interests: synaptic plasticity; NMDAreceptor; autism; endothelial cell; neurovascular coupling; Ca2+ signaling; nitric oxide
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The intimate and dynamic communication between the heart and brain has emerged as a crucial area of investigation in neuroscience and cardiovascular medicine. Once considered as functionally distinct organs, the heart and brain are now recognized as part of an integrated bidirectional axis, interconnected through complex neural, humoral, metabolic, and immune pathways. Disruptions in this dialogue have been implicated in a wide range of disorders, including heart failure, arrhythmias, stroke, depression, and cognitive decline. Mounting evidence demonstrates that alterations in cardiac function can profoundly affect brain structure and activity, while central nervous system dysfunction—including stress, autonomic imbalance, and neuroinflammation—can negatively impact cardiac output and rhythm stability.

This Special Issue aims to explore the multifaceted mechanisms that govern heart–brain crosstalk in both physiological and pathological conditions. Topics of interest include neurocardiology, autonomic regulation, the role of neuroinflammation, cardiac–cerebral syndromes, psychocardiology, and emerging molecular and imaging biomarkers. We are particularly interested in translational approaches that bridge basic science and clinical practice and in innovative therapeutic perspectives targeting this axis.

I am, therefore, pleased to invite all of you to contribute to this Special Issue, “Advances in Heart–Brain Axis”, by submitting your most recent research or theoretical perspectives on the mechanisms linking cardiovascular and central nervous system function. Particular emphasis will be given to the role of calcium signaling, synaptic plasticity, and ion transport in mediating heart–brain interactions under both physiological and pathological conditions. Experimental studies, comprehensive reviews, and insightful commentaries are all warmly welcome.

Dr. Teresa Soda
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • heart–brain axis
  • neurocardiology
  • autonomic nervous system
  • neuroinflammation
  • cardiac–cerebral syndromes
  • psychocardiology
  • calcium signaling
  • synaptic plasticity
  • ion transport
  • translational neuroscience

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Published Papers (5 papers)

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Research

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11 pages, 347 KB  
Article
Acute Effects of Transcutaneous Auricular Vagus Nerve Stimulation on Autonomic Nervous System Regulation and Spasticity in Children with Spastic Cerebral Palsy: A Preliminary Study
by Gulay Yalcin, Gorkem Acar, Muhammed Fatih Kavak, Sevinç Külekçioğlu and Ali Veysel Özden
Biomedicines 2026, 14(6), 1370; https://doi.org/10.3390/biomedicines14061370 - 18 Jun 2026
Viewed by 628
Abstract
Objective: This study aims to investigate the acute effects of transcutaneous auricular vagus nerve stimulation (taVNS) on autonomic nervous system (ANS) regulation and spasticity in children with spastic cerebral palsy (SCP). Methods: This preliminary study includes 20 children aged 2–15 years diagnosed with [...] Read more.
Objective: This study aims to investigate the acute effects of transcutaneous auricular vagus nerve stimulation (taVNS) on autonomic nervous system (ANS) regulation and spasticity in children with spastic cerebral palsy (SCP). Methods: This preliminary study includes 20 children aged 2–15 years diagnosed with SCP. Participants undergo a single session of taVNS. Spasticity is assessed using the Modified Ashworth Scale, and autonomic regulation is evaluated through heart rate variability (HRV) parameters measured before and immediately after stimulation. Results: Following taVNS, spasticity scores decrease significantly (Modified Ashworth Scale: pre 2.00 ± 0.64 vs. post 1.60 ± 0.52; p = 0.004). Significant reductions are also observed in mean heart rate (pre 98.60 ± 16.32 bpm vs. post 91.25 ± 20.22 bpm; p = 0.022), LF/HF ratio (pre 2.22 ± 2.22 vs. post 1.12 ± 0.84; p = 0.006), and LF power (p = 0.009). No significant changes are detected in RMSSD, pNN50, or HF power (all p > 0.05). No adverse events are reported. Conclusions: This preliminary study suggests that a single session of taVNS may be associated with acute changes in autonomic regulation and reductions in spasticity in children with SCP. The observed shifts in HRV parameters indicate a modulation of sympathovagal balance. These findings support the feasibility of taVNS as a non-invasive neuromodulatory approach and warrant further large-scale, controlled studies with longer follow-up. Because of the small sample size, the absence of a control or sham group, and the short (1-min) HRV recording window, these results should be regarded as preliminary and hypothesis-generating, and they require confirmation in larger, randomised, sham-controlled studies. Clinical Trial Registration: This study was registered at ClinicalTrials.gov (Identifier: NCT06880887) on 10 March 2025. The study was conducted between January 2025 and March 2025; registration on 10 March 2025 therefore occurred during the enrolment and data-collection period rather than prior to it. This retrospective registration is acknowledged as a limitation. Full article
(This article belongs to the Special Issue Advances in Heart–Brain Axis)
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18 pages, 1718 KB  
Article
Heart–Brain Temporal Coupling as a Candidate Biomarker of Self-Congruency
by Nicolas Bourdillon, Sébastien Urben, Nina Rimorini, Alicia Rey, Cyril Besson, Jean-Baptiste Ledoux, Yasser Alemán-Gómez, Eleonora Fornari and Solange Denervaud
Biomedicines 2026, 14(3), 548; https://doi.org/10.3390/biomedicines14030548 - 27 Feb 2026
Viewed by 1314
Abstract
Background. Self-congruency refers to the coherence between emotional experience (internal states) and enacted behavior (outward actions). Reduced self-congruency has been linked to vulnerability in mental health, yet its physiological correlates remain poorly characterized. Heart–brain temporal coupling may provide a candidate physiological marker [...] Read more.
Background. Self-congruency refers to the coherence between emotional experience (internal states) and enacted behavior (outward actions). Reduced self-congruency has been linked to vulnerability in mental health, yet its physiological correlates remain poorly characterized. Heart–brain temporal coupling may provide a candidate physiological marker of this psychological coherence. Methods. Thirty-eight healthy adults underwent resting-state functional magnetic resonance imaging while cardiac activity was simultaneously recorded using photoplethysmography to derive heart rate variability (HRV). Self-congruency was assessed using a graphic rating scale based on the spatial overlap between emotional experience and enacted behavior. Heart–brain temporal coupling between HRV and regional blood-oxygen-level-dependent (BOLD) signals was quantified using cross-covariance analysis across biologically plausible temporal shifts. Results. Heart–brain temporal coupling predominantly reflected brain-to-heart temporal ordering, particularly within regions central to the neurovisceral integration model, including the ventromedial prefrontal and anterior cingulate cortices. In contrast, higher self-congruency was associated with stronger heart-to-brain temporal coupling, notably within the right rostral middle frontal gyrus and supramarginal gyrus, regions implicated in emotion regulation and socio-emotional processing. Conclusions. While global heart–brain temporal coupling is dominated by top-down neural regulation, greater alignment between emotional experience and enacted behavior is associated with enhanced bottom-up cardiac temporal ordering on neural activity. These findings seem to identify a physiological–psychological axis that may inform original prevention-oriented approaches in mental health. Full article
(This article belongs to the Special Issue Advances in Heart–Brain Axis)
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Review

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29 pages, 2573 KB  
Review
Voltage-Dependent Ion Channels in Vascular Endothelial Cells: An Unexpected Signaling Pathway in Non-Excitable Cells
by Francesco Moccia and Teresa Soda
Biomedicines 2026, 14(7), 1418; https://doi.org/10.3390/biomedicines14071418 - 23 Jun 2026
Viewed by 525
Abstract
Voltage-gated ion channels (VGICs) are traditionally associated with electrically excitable cells; however, increasing evidence indicates that they are also expressed in non-excitable cells, including vascular endothelial cells. This review aims to summarize the current knowledge on the expression, regulation, and functional role of [...] Read more.
Voltage-gated ion channels (VGICs) are traditionally associated with electrically excitable cells; however, increasing evidence indicates that they are also expressed in non-excitable cells, including vascular endothelial cells. This review aims to summarize the current knowledge on the expression, regulation, and functional role of VGICs in the vascular endothelium, and to highlight their potential contribution to endothelial signaling. We examined the molecular structure, biophysical properties, and functional roles of voltage-gated Na+ (NaV), Ca2+ (CaV), and K+ (KV) channels in vascular endothelial cells. Particular attention was given to studies investigating VGIC activity in native endothelium and to emerging mechanisms regulating their activation. Endothelial cells express multiple VGIC subtypes at low densities, which are insufficient to generate action potentials but can modulate membrane potential (VM) and Ca2+-dependent signaling. The dynamic regulation of the endothelial VM, through the interplay between hyperpolarizing and depolarizing conductances, emerges as a key determinant of VGIC availability and activation. VGICs contribute to essential endothelial functions, including angiogenesis, vasomotor responses, blood–brain barrier permeability, and inflammation. Dysregulated VGIC expression and/or activity may be implicated in several pathological conditions, such as atherosclerosis, calcific aortic stenosis, and tumor vascularization. VGICs represent an unexpected but functionally relevant component of endothelial signaling. Elucidating their role in native vascular beds and disease contexts may uncover novel mechanisms of endothelial regulation and identify new therapeutic targets in cardiovascular and cancer biology. Full article
(This article belongs to the Special Issue Advances in Heart–Brain Axis)
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51 pages, 1917 KB  
Review
Neuroimmune Regulation of Microvascular Inflammation: The Heart–Brain Axis, Mast Cells, and the Protective Role of Flavonoids—A Comprehensive Review
by Paraskevi Papadopoulou and Theoharis C. Theoharides
Biomedicines 2026, 14(5), 1073; https://doi.org/10.3390/biomedicines14051073 - 8 May 2026
Cited by 1 | Viewed by 1986
Abstract
Background/Objectives: Cardiovascular disease (CVD), particularly coronary artery disease (CAD), is increasingly linked to microvascular inflammation driven by interactions between immune, vascular, and neuroendocrine systems. Mast cells (MCs), strategically positioned near blood vessels, play pivotal roles in this process through the release of [...] Read more.
Background/Objectives: Cardiovascular disease (CVD), particularly coronary artery disease (CAD), is increasingly linked to microvascular inflammation driven by interactions between immune, vascular, and neuroendocrine systems. Mast cells (MCs), strategically positioned near blood vessels, play pivotal roles in this process through the release of inflammatory and vasoactive mediators, contributing to increased vascular permeability, endothelial dysfunction, and tissue inflammation in conditions including ischemia–reperfusion (I/R) and CVD. This comprehensive review examines the cellular and molecular mechanisms underlying MC-mediated microvascular inflammation, with emphasis on neuroimmune regulation through the heart–brain axis, and evaluates the therapeutic potential of flavonoids. Methods: A review of in vitro, animal, and clinical studies was conducted to assess MC-mediated cardiovascular pathology and the pharmacological effects of natural flavonoids on MC activation and microvascular inflammation. Results: Psychological and physical stress activates hypothalamic corticotropin-releasing hormone (CRH) signaling, directly triggering coronary MC degranulation via CRHR-1 and CRHR-2 receptors, while co-released neuropeptides, including neurotensin and urocortin, amplify this neuroimmune cascade. Traumatic brain injury, autonomic dysregulation, and atrial fibrillation further perpetuate this bidirectional heart–brain axis, linking neurological stress to microvascular injury and adverse cardiac remodeling. An autocrine–paracrine CRH amplification loop sustains chronic coronary microvascular inflammation, contributing to heart failure with preserved ejection fraction (HFpEF) and MC activation disease (MCAD)-related cardiovascular manifestations. Natural flavonoids were found to inhibit MC activation, suppress inflammatory mediator synthesis, and protect microvascular integrity through multiple molecular targets, including calcium signaling, transcription factors, oxidative stress pathways, and CRHR-1-mediated neuroimmune signaling. Conclusions: While challenges remain regarding bioavailability and standardization, multi-compound formulations targeting multiple risk factors hold promise for preventing CVD progression. Future research directions for advancing these natural compounds toward clinical implementation are identified. Full article
(This article belongs to the Special Issue Advances in Heart–Brain Axis)
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38 pages, 1910 KB  
Review
The Bidirectional Relationship Between Myocardial Infarction and Depression: Risk Factors, Mechanisms, and Interventions
by Zhuorui Cui, Qiaoning Yang, Furong Yang, Yankai Yang, Xuexin Yang, Yanqiao Yu, Yajie Cai, Xiaodi Fan and Ruina Bai
Biomedicines 2025, 13(11), 2838; https://doi.org/10.3390/biomedicines13112838 - 20 Nov 2025
Cited by 2 | Viewed by 3338
Abstract
Myocardial infarction (MI) and depression exhibit a bidirectional relationship, in which patients with MI are more susceptible to depression, and individuals with depression face a heightened risk of MI. The two diseases are intricately intertwined via the heart–brain axis. Sex, age, lifestyle, social [...] Read more.
Myocardial infarction (MI) and depression exhibit a bidirectional relationship, in which patients with MI are more susceptible to depression, and individuals with depression face a heightened risk of MI. The two diseases are intricately intertwined via the heart–brain axis. Sex, age, lifestyle, social background, comorbidities, and genetics contribute to and affect the prognosis of this combined condition. Mechanisms involving the autonomic nervous system (ANS), hypothalamic–pituitary–adrenal (HPA) axis, inflammation, thrombosis, tryptophan metabolism, renin–angiotensin–aldosterone system (RAAS), endothelial dysfunction, microRNAs, and gut microbiota, as components of the heart–brain axis, have been implicated in the pathological link between MI and depression. This review outlines the common risk factors and potential mechanisms underlying this bidirectional relationship. It treats the comorbidities of MI and depression as a unified condition, relying on evidence from clinical trials and experimental studies that directly address both diseases together rather than extrapolating from separate studies on MI or depression alone. It also discusses current therapeutic approaches, including non-pharmacological interventions like psychotherapy and exercise, and pharmacological treatments with chemical or natural compounds. Finally, this review identifies significant gaps in the pathophysiology and clinical management of MI with depression, which warrant further investigation. Full article
(This article belongs to the Special Issue Advances in Heart–Brain Axis)
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